Respiratory Physiotherapy An On Call Survival Guide Physiotherapy pocketbooks Second Edition, jennifer pryor

The management of volume loss 89 7 ● Increased airway resistance. At low lung volumes all air-containing compartments, including the airways, reduce in size. Thus airway resistance increases as lung volume decreases. Remember FRC is important to preserve the surface area for: ● gas exchange ● V/Q matching and therefore oxygenation. TIDAL VOLUME Tidal volume (VT), a normal adult breath, is approximately 500 ml. Tidal breathing starts and finishes at FRC (see Fig. 7.1). Causes of decreased VT ● An increase in airway resistance, e.g. bronchospasm, bronchial inflammation ● A decrease in lung compliance, e.g. pleural effusion, fibrosing alveolitis ● A decrease in chest wall compliance, e.g. neuromuscular disorders, pain ● Depression of respiratory drive, e.g. excessive narcotic analgesia. Consequences of decreased VT a. reduction in alveolar ventilation (hypoventilation) [Alveolar ventilation = VT (less dead space) × respiratory rate] b. carbon dioxide retention and respiratory acidosis c. hypoxia, if alveolar ventilation is reduced and/or metabolic needs of the body are increased. FORCED VITAL CAPACITY FVC is the amount of air that can be forcefully expelled from maximal inspiration to maximal expiration (see Fig. 7.1). Causes of decreased FVC ● Compromised inspiratory capacity, e.g. reduced inspiratory muscle strength, obesity ● Compromised expiratory capacity, e.g. reduced expiratory muscle strength, increased airways resistance ● Depression of respiratory drive, e.g. neurological impairment.

7 90 The management of volume loss Consequences of decreased FVC ● Decreased forced expiratory flow rate leading to less effective forced expiration manoeuvres Remember VT and FVC are important for: ● CO2 clearance ● oxygenation ● the ability to huff or cough effectively. ASSESSING VOLUME LOSS Consider these questions: ● Which lung volumes are affected (FRC, VT, FVC) ● Is it generalized or localized? ● Is it: a. acute b. chronic c. acute on chronic loss? ● Which pathophysiological mechanisms are responsible? Why has the patient got volume loss? Understanding the underlying pathophysiological mechanisms guides appropriate management (Table 7.1). Working out the problem The signs of the different types of volume loss may mimic each other making it difficult to identify the underlying cause. Table 7.2 lists each of the possible causes together with key assessment ‘clues’ which should enable the clinician to formulate a working clinical diagnosis. The table also includes a suitable assessment tool for evaluation of treatment success. Key point of treatment Once the clinical diagnosis has been correctly established then the following principles of treatment could apply (Boxes 7.1, 7.2, 7.3). VOLUME LOSS – MANAGEMENT BY DIAGNOSIS See Table 7.3.

The management of volume loss 91 Table 7.1 Underlying pathophysiological mechanisms of volume loss ↓Lung volume due to Which primary Cause volume affected Intrusion of abdominal contents into chest ↓FRC Position, intestinal obstruction, ascites, paralytic ileus, obesity, congenital defect of the diaphragm, diaphragm paralysis Abnormalities of the ↓FRC Pneumothorax, pleural effusion, empyema, pleural space haemothorax Decrease in chest wall ↓VT, FVC, FRC Skeletal problems: compliance a. kyphoscoliosis b. ankylosing spondylitis Neuromuscular problems: fatigue due to 7 increased WOB (length–tension inappropriateness); dystrophies; motor neurone disease; myopathies; spinal injuries; cardiovascular accident (stroke) Airway obstruction ↓FVC Secretions, inflammation, collapse, tumour, oedema, bronchoconstriction, foreign body (NB: paediatrics – foreign body may cause increase lung volume, i.e. ball valve effect) Abnormality of lung tissue ↓FRC Pneumonia, consolidation, upper abdominal and cardiothoracic surgery, interstitial lung disease, collapse, ARDS Loss of respiratory drive ↓VT, FVC Neurological impairment, excessive narcotic analgesia Other factors ↓VT, FVC Pain (incisional/pleuritic, fractures), fear Remember ● Do not apply CPAP if the patient is retaining CO2 – CPAP does not alter VT and may cause further CO2 retention and the patient will become more acidotic. ● Consider NIV if the patient is in Type I respiratory failure with a low CO2 – this may indicate that the patient is working excessively hard, prior to type II respiratory failure. ● Positioning a patient with profound volume loss for treatment may cause desaturation (due to V/Q mismatch) – discuss with the medical team the risk/benefit of increased oxygen therapy while in the position; avoid posi- tions that compromise oxygen saturations if supplementary oxygen is not appropriate.

7 Table 7.2 Signs and symptoms of volume loss 92 The management of volume loss Condition History Chest wall CXR Arterial Auscultation RR Lung volume Assessment ARDS/ALI movement ↑ affected tool Widespread alveolar blood gases FRC PaO2 Consolidation/ shadowing pneumonia Many predisposing ? reduced ↓PaO2 Fine SpO2 factors ↓SpO2 inspiratory ?↑PaCO2 crackles FRC PaO2 SpO2 Surgery ? ↓over area ↑opacity (whiter) air ↓PaO2 Bronchial ↑ or Percussion Infection breathing N/A note Immobility bronchograms ↓SpO2 (BB) Aspiration Loss of silhouette sign Collapse Surgery ?↓ Raised ↓PaO2 ↓BS in ↑ or FRC Auscultation Generalized Obesity hemidiaphragms ↓SpO2 dependent N/A CXR Prolonged areas PaO2 dependent ? opacity in the SpO2 atelectasis recumbency dependent areas ? BB Collapse Pain ? ↓ ↑opacity ↓PaO2 Absent BS ↑ FRC Auscultation Lobar Sputum plugging over area loss of silhouette sign ↓SpO2 ? BB if CXR Incorrect Shift of structures patent PaO2 airway SpO2 endotracheal towards opacity tube position

Condition History Chest wall CXR Arterial Auscultation RR Lung volume Assessment Flail chest movement ↑ affected tool Pain Chest wall Paradoxical Rib fractures blood gases Pleural effusion trauma/RTA/fall Possible evidence VT PaO2 ↓PaO2 ↓BS FVC SpO2 Pneumothorax of lung contusion ↓SpO2 (↑opacity) Recent surgery ↓ Poor inspiratory effort ↑PaCO2 ↓BS ↑ VT VAS Trauma FVC Observation ↓Lung volume ? ↓PaO2 PaCO2 ↑ FRC Recent surgery Normal ↑opacity Normal ↓BS if CXR Malignancy May be Meniscal sign large Percussion Heart failure Fluid line if erect film Fluid overload reduced if note large (crisp line if air effusion present) Trauma ↓ ↑Translucency ↓PaO2 ↓BS or ↑ FRC CXR Central line Normal (blacker) ↓SpO2 absent BS ? VT RR PaO2 insertion May be shift of Normal (if SpO2 The management of volume loss 93 Chest drain structures away small) Percussion from translucency removal note (occasionally Increased definition/ Subcutaneous caused by drain crispness of heart being put in to border or diaphragm emphysema drain an indicating anterior effusion) and/or basal Idiopathic pneumothorax 7

7 Table 7.2 Continued 94 The management of volume loss Condition History Chest wall CXR Arterial Auscultation RR Lung volume Assessment movement ↑ affected tool N/A blood gases FRC CXR ? VT Pulmonary oedema Evidence of heart Widespread alveolar ↓PaO2 Late fine failure/renal shadowing ↓SpO2 inspiratory ? VT PaCO2 failure/positive Bilateral hilar flare crackles, FVC FVC fluid balance wheeze FRC ? enlarged heart ? small effusions seen or fluid in fissures visible Respiratory muscle Medical diagnosis ↓ Poor inspiratory effort ↑PaCO2 ↓BS ↑ ↓Lung volumes ? ↓PaO2 or weakness/ Extensive period of ? Paradoxical ↓SpO2 ↓ fatigue ↑RR if phrenic Spirometry – ↓FVC nerve Prolonged weakness/ ventilatory paralysis support

The management of volume loss 95 7 Box 7.1 Treatment strategies for reduced FRC Aim: To increase FRC ● Positioning to optimize FRC, V/Q and diaphragm length–tension relationship ● CPAP ● Controlled mobilization with breathing strategies ● If ventilated, increase PEEP Box 7.2 Treatment strategies for reduced tidal volume Aim: To increase tidal volume ● Breathing exercises: lower thoracic expansion exercises (LTTEs). Infants cannot significantly increase their tidal volumes so will increase their RR to increase their MV ● Incentive spirometry. In children, blowing games: bubbles/windmills, bubble PEP ● Controlled mobilization with breathing strategies ● IPPB/NIV ● Neurophysiological facilitation techniques ● If ventilated, manual hyperinflation/ventilator hyperinflation when appropriate Box 7.3 Treatment strategies for localized static volume loss, e.g. lobar collapse Aim: To reverse atelectasis ● Positioning to optimize FRC, V/Q and diaphragm length–tension relationship ● Advise regarding optimization of O2 therapy ● Breathing exercises, LTEEs, inspiratory hold, sniff – collateral ventilation, which is not well developed in infants ● Incentive spirometry. In children, blowing games: bubbles/windmills, bubble PEP ● IPPB ● CPAP if good tidal volume ● Controlled mobilization ● Neurophysiological facilitation techniques ● If ventilated, manual hyperinflation ● If secretions present (see Ch. 6)

7 Table 7.3 Management by diagnosis 96 The management of volume loss Diagnosis Volume lost Treatment options Self-ventilating Ventilated ARDS/acute lung ↓FRC ● Ensure optimization of O2 therapy ● Positioning – side-lying (abdomen free), ?prone injury ● Positioning – erect sitting, side-lying (abdomen free) ● Avoid any manoeuvres which involve ● CPAP/NIV disconnecting the patient from the ventilator to preserve PEEP Consolidation/ ↓FRC ● Ensure optimization of controlled O2 therapy. If severe ● Positioning: pneumonia hypoxaemia may require CPAP or NIV Adults – side-lying (abdomen free) with unaffected lung down ● Positioning: Paediatrics – side-lying with affected lung down Adults – side-lying (abdomen free) with unaffected lung down ● When/if become productive, use sputum Paediatrics – side-lying with affected lung down clearance techniques When/if become productive, use airway clearance techniques ● Paediatrics – may tolerate having the affected lung up which would help drain any loose ● Humidification secretions and encourage ventilation to that lung. As in all patients, need to assess individual’s tolerance to handling/treatment Collapse ↓FRC ● Ensure optimization of controlled O2 therapy. If severe ● Recruitment manoeuvres – PEEP, manual hypoxaemia may require CPAP or NIV hyperinflation and inspiratory hold ● Positioning: ● Positioning in high side-lying (abdomen free) Adults – high sitting (bed or chair), side-lying ● Reverse Trendelenburg (feet down, whole bed tilt) (abdomen free) ● Adults – instillation of 0.9% NaCl if sputum Paediatrics – as tolerated and manual techniques/ blowing games in younger patients plugging Paediatrics – ? selective mini-lavage (if trained) ● Mobilization with breathing strategies if sputum plugging

Table 7.3 Continued Diagnosis Volume lost Self-ventilating Treatment options Collapse lobar ↓FRC Ventilated ● Ensure optimization of controlled O2 therapy. If severe ● Positioning: The management of volume loss 97 hypoxaemia may require CPAP or NIV Adults – side-lying (abdomen free) with unaffected lung down (optimize V/Q & GAP) ● Positioning: Paediatrics – side-lying with affected lung down Adults – side-lying (abdomen free) with unaffected (optimize V/Q) lung down (optimize V/Q & GAP) Paediatrics – side-lying with affected lung down ● Manual hyperinflation maintaining PEEP (optimize V/Q) ● Inspiratory hold May need to have affected lung up to drain. If poorly ● If sputum retention use airway clearance tolerated short, frequent treatments. Then when improving may tolerate being left with techniques affected lung up to increase ventilation to that Paediatrics – selective mini-lavage (if trained). lung If upper lobe problem – sit up provided ETT is ● TEEs with inspiratory holds well secured ● Neurophysiological facilitation techniques ● Incentive spirometry (IS) ● IPPB ● If sputum retention use airway clearance techniques 7

7 Table 7.3 Continued 98 The management of volume loss Diagnosis Volume lost Treatment options Flail chest Self-ventilating Ventilated ↓VT ● Liaise with medical staff to ensure optimal pain ● Positioning: control Adults – high sitting or side-lying (abdomen free) ● Ensure optimization of controlled O2 therapy with unaffected lung down ● Positioning: Paediatrics – high sitting or side-lying with Adults – side-lying (abdomen free) with unaffected affected lung down but lying on affected side lung down (optimize V/Q) may be more painful and lead to decreased Paediatrics – side-lying with affected lung down ventilation (unless patient paralysed and fully (optimize V/Q) ventilated with adequate analgesia) ● CPAP or NIV to ‘splint’ the chest wall ● If sputum retention use airway clearance ● TEEs with inspiratory holds techniques ● Neurophysiological facilitation techniques ● IPPB – avoid use until pneumothorax excluded ● If sputum retention use airway clearance techniques Pain ↓VT ● Liaise with medical staff to ensure optimal pain ● Lung volumes will not be affected if adequately ↓FVC control sedated, analgesed and fully ventilated ● Long acting – e.g. PCA ● If on an assisted mode of ventilation, i.e. Short acting – bolus of opioid, Entonox pressure support & PEEP then: Regional analgesia Liaise with medical staff to ensure optimal pain ● Relaxation techniques control ● Reassurance Long acting – e.g. PCA if awake Short acting – bolus of opioid ● Relaxation techniques ● Reassurance

Table 7.3 Continued Diagnosis Volume lost Treatment options Pleural effusion Self-ventilating Ventilated ↓FVC ● Positioning: ● Positioning: ↓VT if large Adults – side-lying (abdomen free) with unaffected Adults – side-lying (abdomen free) with unaffected lung down (optimize V/Q) lung down (optimize V/Q) Paediatrics – side-lying with affected lung down Paediatrics – side-lying with affected lung down (optimize V/Q) (optimize V/Q) ● NB if pleural effusion very large then the above ● Liaise with medical team regarding insertion of positioning may cause further volume loss – alter to ICD supported high sitting ● Ensure optimization of controlled O2 therapy ● Liaise with medical team regarding insertion of inter-costal chest drain (ICD) Pneumothorax ↓FVC ● Liaise with medical team regarding insertion of ICD ● Liaise with medical team regarding insertion of ICD ● Ensure optimization of controlled O2 therapy ● Ensure optimization of controlled O2 therapy Pulmonary ↓FVC The management of volume loss 99 oedema ● Ensure optimization of controlled O2 therapy ● PEEP ● CPAP ● Paediatrics – pulmonary oedema may be quite ● NIV with CPAP facility ● Medical treatment sticky and may potentially cause small airways to ● Positioning in high side-lying (abdomen free) block ● Reverse Trendelenburg (feet down, whole bed tilt) Respiratory ↓FVC ● Fully supported positioning including shoulder girdle ● IPPB muscle ↓VT ● NIV weakness/fatigue 7

7 100 The management of volume loss Key messages ● Identify which lung volumes are reduced and select the strategy that requires the minimum intervention to produce the required outcome. ● Strategies should also include those that can easily be performed independently by the patient or with the help of the nurse. Further reading Berne RM, Levy MN (2000) Principles of physiology, 3rd edn. St Louis, MO: Mosby. Hough A (2001) Physiotherapy in respiratory care: an evidence-based approach to respiratory and cardiac management, 3rd edn. Cheltenham: Nelson Thornes. Lumb AB (2005) Nunn’s applied respiratory physiology. Philadelphia, PA: Elsevier, Butterworth-Heinemann. Pryor JA, Prasad A (2002) Physiotherapy for respiratory and cardiac problems, 3rd edn. London: Churchill Livingstone. West J (2004) Respiratory physiology: the essentials. Philadelphia, PA: Lippincott, Williams and Wilkins.

The management of increased CHAPTER 8 work of breathing Alison Aldridge This chapter describes the management of patients with increased work of breathing. Work of breathing (WOB) = the rate of oxygen consumption of the respiratory muscles During quiet respiration: ● The work of breathing is performed entirely by the inspiratory muscles. ● Expiration is passive, powered by the elastic recoil of the tissue. ● As breathing becomes more difficult the muscles work harder and thus the WOB increases. The efficiency of the respiratory muscles is reduced in patients presenting with: ● respiratory disease ● thoracic deformities ● severe obesity, ascites, pregnancy, etc. ● cardiac disease ● cerebral lesions ● sepsis, etc. Many patients cope with this reduced respiratory muscle efficiency, until some- thing else happens, e.g. chest infection. This results in a much faster deterioration than normal. CLINICAL SIGNS See Table 8.1. BRONCHOSPASM Bronchospasm is exacerbated by cold, anxiety, dehydration, infection and hypoxia (Table 8.2).

102 The management of increased work of breathing Table 8.1 Clinical features of increased work of breathing Adult (>16 years) Clinical features of increased work of breathing 8 Respiratory ● ↑RR (dyspnoea) ● ↓HR (tachycardia) ● Mouth breathing ● Altered depth and pattern of breathing (e.g. deep, shallow, irregular, apnoeas, pursed lip breathing) ● Accessory muscle use ● Reduced SpO2 ● Deranged arterial blood gases ● Carbon dioxide retention (hypercapnia) may cause: a. peripheral vasodilation; warm hands b. bounding pulse c. flapping tremor of hands ● Secondary signs: a. cerebral – restlessness/irritability/confusion/seizure/ coma b. cardiac – tachycardia/hypertension/bradycardia/ hypotension/cardiac arrest c. fatigue Child (>2 years) Respiratory The clinical signs are comparable with those in adults with the following age-related differences: ● ↑RR (tachypnoea) [2–6 years normal 20–40] [>6 years normal 15–30] ● Intercostal recession ● Nasal flaring ● Expiratory grunting ● Tracheal tug The secondary systemic clinical signs are similar to those in adults with the following age-related cardiac differences: ● ↑HR (tachycardia) [normal 60–140] ● ↑BP (hypertension) [normal 95–105/53–66] Baby (newborn–2 years) Respiratory Clinical signs are comparable to those of a child with the following age-related differences: ● ↑RR (tachypnoea) [newborn normal 30–50 b.p.m.] [<2 years normal 20–40 b.p.m.] ● ↑HR (tachycardia) [newborn normal 80–200 b.p.m.] [<3 years normal 100–190 b.p.m.] ● ↑BP (hypertension) [newborn normal 50–70/25–45] [<2 years normal 87–105/53–66]

The management of increased work of breathing 103 Table 8.2 Treatments and suggested modifications for bronchospasm Adult Suggested treatment options and modifications ● Check effective bronchodilator therapy, e.g.: 8 a. check technique, regular administration and compliance b. nebulizer therapy requires an adequate tidal volume for effective delivery to the airways – the breathless patient may not receive a therapeutic dose due to small breath size c. intravenous delivery may be more effective (however, potential cardiac side-effects) ● Use breathlessness positioning to aid relaxation, e.g. forward-lean sitting ● Ensure adequate, controlled oxygen therapy ● Humidified oxygen therapy should be prescribed ● Heated humidification if cold system fails to alleviate bronchospasm ● Ensure any retained secretions are cleared effectively ● Active cycle of breathing techniques (ACBT). Emphasis upon breathing control, care with FET as the irritability of the airways may lead to spasms of coughing ● Avoid manual techniques; single-handed, slow rhythmical percussion can be useful, although evidence is lacking ● Intermittent positive pressure breathing (IPPB): a. the system should be set up according to local hospital policy and you should only set up and use this equipment if you have been specifically trained and assessed as competent to do so b. bronchodilators can be used in the nebulizer c. use with high flow rate for patient comfort d. try to get patient to rest and let the machine do the work once the breath is triggered Note: Discontinue immediately if bronchospasm worsens ● Non-invasive ventilation (NIV): a. the system should be set up according to local hospital policy and you should only set up and use this equipment if you have been specifically trained and assessed as competent to do so b. make sure patient comfortable and reassured c. let patient hold mask to face before being strapped in so that they feel in control d. encourage patient to relax and let the machine help them e. you are aiming to rest the respiratory muscles f. stay with the patient while they become accustomed to the machine

104 The management of increased work of breathing Table 8.2 Continued Suggested treatment options and modifications Note: Discontinue immediately if bronchospasm worsens 8 ● Continuous positive airway pressure (CPAP): a. the system should be set up according to local hospital policy and you should only set up and use this equipment if you have been specifically trained and assessed as competent to do so b. in severe asthma hyperinflation of the lungs is common c. in an acute exacerbation, hyperinflation increases as does the WOB d. CPAP takes over the effort of maintaining this sustained inspiratory activity and keeps the airways open during expiration, thus allowing greater gas emptying e. commonly only low pressures are required, 5 cmH2O, and should be prescribed by medical team, as should the required oxygen level f. the system should be set up according to local hospital policy g. a heated humidification system is recommended Note: The use of positive pressure in the presence of bronchospasm is controversial and can be technically challenging. It should be undertaken only if discussed with senior medical staff and if you are trained and competent to do so. Child ● As above ● Unless using a nebulizer, children between 3 and 5 years are recommended to use an inhaler and spacer; those over 10 years may use a metered dose inhaler ● Consider the use of IPPB in the older child (6 years or older) Baby ● As above ● Bronchodilator therapy. Unless using a nebulizer, children under 2 years are recommended to use an inhaler with spacer and mask ● Heated humidification is commonly used in the non-intubated baby

The management of increased work of breathing 105 DISRUPTION OF THE MECHANICS OF THE THORACIC CAGE See Tables 8.3 and 8.4. HYPERCAPNIA (PaCO2): TYPE II RESPIRATORY FAILURE See Table 8.5 and refer also to Chapter 9. Table 8.3 Disrupted integrity of the thoracic cage Adult Suggested treatment options and modifications ● Adequate analgesia ● Controlled oxygen therapy ● Adequate humidification ● CPAP to stabilize a flail segment Child ● As above, although compliance with CPAP is likely to be poor in younger children 8 ● Phrenic nerve damage is a recognized complication post paediatric cardiac surgery resulting in elevation of the diaphragm on the affected side, compression of the lower lobe and persistent collapse ● Physiotherapy is directed towards the management of sputum retention and postoperative atelectasis Baby ● As above; however, in infants prolonged ventilation may be necessary and physiotherapy is directed to managing the presenting problems Table 8.4 Respiratory muscle weakness Adult ● Phrenic nerve damage is a recognized complication post cardiac surgery resulting in elevation of the diaphragm on the affected side, compression of the lower lobe and persistent collapse ● Neuromuscular weakness affecting the respiratory muscles will gradually present as type II respiratory failure (CO2) due to increasing hypoventilation ● Inadequate nutrition especially in the presence of a prolonged high metabolic rate (e.g. HIV, cancer) decreases the ability to sustain increased respiratory effort – early ventilatory support is beneficial Child ● As above Baby ● As above

106 The management of increased work of breathing Table 8.5 Treatments and suggested modifications for type II respiratory failure Adult Suggested treatment options and modifications 8 ● Hypercapnia PaCO2 >6.0 kPa ● Consider treatment options for: a. eliminating the identified cause of the hypoventilation, i.e. sputum retention, bronchospasm, etc. b. managing the cause of the hypoventilation, e.g. thoracic/spinal deformity, muscle weakness, distended abdomen, which leaves the patient unable to compensate for a respiratory problem. Ventilatory support is often needed during the acute illness ● Monitor CO2 and pH regularly. pH below normal levels must be treated – by managing the cause of hypoventilation. Use arterial blood gases or non- invasive transcutaneous CO2 gas monitoring (if available) ● IPPB. The positive effects of IPPB sessions should be carried over with regular ACBT if possible. You may need to treat the patient little and often. Excellent results are possible with IPPB if NIV is not available to you ● NIV is an effective treatment to increase CO2 washout, by increasing tidal volume, if available; this must be discussed with the medical team Child ● As above, hypercapnia PaCO2 >6.0 kPa ● Early detection of mild hypercapnia can be managed by either IPPB or NIV ● The choice of machine and ventilatory setting should be discussed and agreed with the medical team ● Close monitoring of CO2 is essential ● Severe, acute deterioration will require urgent transfer to the paediatric intensive care unit ● Treatment planning will then be directed at eliminating the identified cause of the hypoventilation, i.e. sputum retention, bronchospasm, etc. Baby ● Hypercapnia PaCO2 >5.0 kPa ● While some NIV machines are suitable for babies, hypercapnia in the very young requires urgent transfer to the paediatric intensive care unit ● Treatment planning is comparable to that for a child, as above HYPOXIA (LOW O2): TYPE I RESPIRATORY FAILURE See Table 8.6 and refer also to Chapter 9. VOLUME LOSS (STATIC AND DYNAMIC) See Table 8.7. POSTOPERATIVE RESPIRATORY DYSFUNCTION The treatment options assume the patient is self-ventilating. Refer to the appropri- ate chapters for intubated patients (Table 8.8).

The management of increased work of breathing 107 Table 8.6 Treatments and suggested modifications for type I respiratory failure Adult Suggested treatment options and modifications ● Treat the cause of the low O2 (hypoxia) 8 ● Continuous saturation monitoring and arterial blood gases as indicated. Saturation monitoring requires good peripheral circulation. Be aware that accuracy is limited by movement, ambient light, nail varnish, as well as underlying pathologies, e.g. anaemias, jaundice, poor peripheral circulation, etc. ● Controlled oxygen therapy to maintain SpO2 > 90% (Check against current BTS guidance) ● Humidification ● Positioning to maximize V/Q ● If PaO2 remains around 8 kPa despite FiO2 0.6 (60%), discuss with medical team. Depending upon assessment findings, consider: a. 100% oxygen, rebreathe bag (remember to close valve to fill bag before use) b. IPPB to increase tidal volume (VT), or c. CPAP to maximize functional residual capacity (FRC) and oxygenation d. these patients may need to be in a high-dependency environment e. ensure oxygen is available once CPAP/IPPB is removed Child ● Continuous saturation monitoring and arterial blood gases as indicated. The medical team must be made aware of any change in condition ● Controlled oxygen therapy to maintain SpO2 at 93–98% ● Nasal cannulae are rarely tolerated in young children ● If PaO2 remains 8 kPa despite FiO2 0.5 (50%), consider CPAP; however, careful consideration must be given to mechanical support depending on the underlying cause and tolerance of the child Baby ● Monitor as above ● Controlled oxygen therapy. In very young babies it is preferable to maintain the FiO2 0.6 to minimize risks of oxygen toxicity; discontinue therapy as soon as possible ● Possible methods of delivery are canopy tent, head box, incubator or mask ● Heated humidification is essential Table 8.7 Treatments and suggested modifications for volume loss Adult Suggested treatment options and modifications ● See chapter on volume loss ● Appropriate positioning is essential ● Treatment should be directed at the primary cause Child ● As above Baby ● As above

108 The management of increased work of breathing Table 8.8 Treatments and suggested modifications for postoperative respiratory dysfunction Adult Suggested treatment options and modifications ● Adequate analgesia ● Positioning to improve functional residual capacity and distribution of ventilation ● Early ambulation ● Thoracic expansion exercises with emphasis on 3-second ‘hold’ and inspiratory ‘sniff’ to increase tidal volume and collateral ventilation ● Incentive spirometry ● IPPB if tidal volume still reduced despite above therapies ● CPAP if PaO2 and FRC still reduced despite above therapies Child ● As above, although care with IPPB and CPAP as compliance may be extremely poor Baby ● Adequate analgesia. Encourage positioning through play and normal developmental activities, rolling, prone position, etc. 8 ● Blowing games in the older baby to facilitate sputum clearance ● Severe dysfunction will require prolonged ventilation and physiotherapy is directed to managing the presenting problems Table 8.9 Treatments and suggested modifications for pulmonary oedema Adult Suggested treatment options and modifications ● Controlled oxygen therapy ● Positioning ● CPAP. Discuss with the medical team the level of PEEP and FiO2 to be prescribed ● Severe sudden onset of pulmonary oedema will require full ventilatory support and is a medical emergency Child ● Management depends on severity of the pulmonary oedema ● In older children with mild oedema the adult options may be considered. However, if the intrapulmonary shunt is large the child, whatever age, will require urgent transfer to intensive care for mechanical ventilatory support Baby Usually a medical emergency due to the large intrapulmonary shunt generated PULMONARY OEDEMA Although the pathophysiological cause is not remediable to physiotherapy the consequent hypoxaemia, dyspnoea, tachypnoea and anxiety may respond to intervention while the pharmacological management takes effect (Table 8.9).

The management of increased work of breathing 109 8 SPUTUM RETENTION Refer to Chapter 6 for the management of sputum retention. In relation to an acute exacerbation of COPD where sputum retention is the primary cause of an increased WOB, there is evidence to support the short-term use of oral mucolytics (erdosteine or carbocisteine) in the early resolution of symptoms. Whilst this may not be an immediate on call issue it may be raised during the post on call handover for further consideration by the medical team. Key messages ● Physiotherapy has a pivotal role in the management of increased work of breathing. ● In order to problem-solve and apply clinical reasoning to treatment planning it is easiest to consider that ventilation is the result of a series of interactions between the central control mechanisms, the respiratory muscles, the skeletal structures they influence and the lung tissue itself. ● An increase in the work of breathing may be caused by dysfunction at any one level but it cannot be analysed in isolation, as respiratory mechanics are dynamic in nature. ● Physiotherapy intervention may be directed at more than one point of the system, as dysfunction at one level may disturb, or be compensated for at, other levels. ● The skill is to analyse the major cause of the disruption, based on the presenting clinical features and the results of any relevant clinical investigations, and then decide at which level the chosen treatment will be most effective. Further reading Hough A (2001) Physiotherapy in respiratory care: a problem solving approach to respiratory and cardiac management, 3rd edn. Cheltenham: Stanley Thornes. Prasad SA, Hussey J (1995) Paediatric respiratory care: a guide for physiotherapists and health professionals. London: Chapman & Hall. Pryor JA, Prasad SA (eds) (2002) Physiotherapy for respiratory and cardiac problems, 3rd edn. London: Churchill Livingstone.



CHAPTER 9 Management of respiratory failure Sarah Keilty Respiratory failure is demonstrated in arterial blood gas (ABG) tensions. Type I respiratory failure is defined by a PaO2 <8.0 kPa with a normal or lowered PaCO2. Type II respiratory failure (ventilatory failure) is defined by a PaO2 <8.0 kPa and a PaCO2 >6.0 kPa. Acute respiratory failure is related to respiratory distress, with increased work of breathing and deranged gas exchange. It may occur with or without the presence of excessive pulmonary secretions and/or sputum reten- tion, and is not necessarily related to a primary respiratory problem, e.g. neurologi- cal problems may be related to respiratory depression, hypoventilation, reduced level of conciousness and inability to protect the airway. Cough depression and risk of aspiration are a serious concern. Unrecognized respiratory failure leads to: ● respiratory muscle fatigue ● hypoventilation ● sputum retention ● ↓O2 (hypoxaemia). Accurate assessment to establish the underlying cause is imperative as, if left untreated, it may progress to any or all of the following: ● cardiac arrhythmia ● cerebral hypoxaemia ● respiratory acidosis ● CO2 narcosis ● coma ● cardiorespiratory arrest. Thus timely recognition and treatment of acute respiratory failure is of the utmost importance and a serious part of patient care on call. HYPOXAEMIA (TYPE I RESPIRATORY FAILURE) Hypoxaemia is defined as inability to maintain the PaO2 above 8 kPa. See Box 9.1 and Table 9.1.

112 Management of respiratory failure Box 9.1 Types of respiratory failure Respiratory failure is classified in two categories: ● Type I respiratory failure: characterized by the inability to maintain an adequate PaO2 (hypoxaemia) but the PaCO2 is normal (or slightly reduced) ● Type II respiratory failure (ventilatory failure): characterized by a reduced PaO2 and, in addition, the PaCO2 has risen above normal levels (hypercapnia) Table 9.1 Classification and causes of hypoxaemia Classification Cause Hypoxic hypoxaemia 9 ● Where blood flows through parts of the ● Primary respiratory disease: COPD, lung which are unventilated pulmonary fibrosis, CF, pneumonia, sputum retention, ↓gas transfer across ● Inability to transfer oxygen across the the thickened (fibrotic/oedematous) pulmonary membrane (gas diffusion respiratory membrane limitation) ● Primary cardiac disease: heart failure, ● Acute bronchoconstriction: asthma congestive cardiac failure, pulmonary (insufficient gas flow in and out of the oedema (causing a diffusion limitation lung) across the respiratory membrane) ● Insufficient inspired oxygen therapy (including faulty oxygen delivery equipment) Ischaemic hypoxaemia: ● Usually due to inadequate blood flow ● Pulmonary embolus through the lung ● Destruction of the pulmonary vasculature (COPD, pulmonary trauma) Anaemic hypoxaemia: ● Reduction in oxygen carrying capacity of ● Shock (significant blood loss with a the blood reduced Hb) ● Primary haematological diseases, e.g. sickle cell crisis, anaemia Toxic hypoxaemia: ● Difficulty in oxygen utilization – common ● E.g. carbon monoxide poisoning, cyanide in patients admitted with inhalation poisoning burns/smoke inhalation injury

Management of respiratory failure 113 CLINICAL SIGNS OF HYPOXAEMIA A patient with hypoxaemia will display: ● central cyanosis (blue lips, tongue) ● peripheral shut-down (cool to touch, ‘cold and clammy’) ● tachypnoea – increased respiratory rate (>20 breaths per minute) ● tachycardia (heart rate >100 bpm) ● low oxygen saturation (<90%) ● confusion or agitation if profound hypoxaemia; may not comply with treatment. AIM OF PHYSIOTHERAPY IN HYPOXAEMIA ● To identify and treat if appropriate the cause of the hypoxaemia, thus aiming to increase the PaO2 > 8.0 kPa while administering appropriate oxygen therapy. TREATMENT OF HYPOXIA 9 The primary treatment for hypoxia is controlled oxygen therapy, plus identification and treatment of the underlying cause. Patients who are unable to maintain SaO2 >90% on facemask oxygen may require additional respiratory support, either continuous positive airway pressure (CPAP) or intubation and mechanical ventila- tion. See Table 9.2 for treatment advice in hypoxaemia and Table 9.3 for common issues in hypoxaemia. Patients with unilateral lung disease can be positioned in side-lying, with the unaffected lung down, to try to improve V/Q matching. Table 9.2 Common treatments for hypoxia Common treatments Advice Controlled oxygen therapy ● Oxygen is a drug which should be prescribed for the required percentage and/or flow rate ● Usually 24–60% can be given by an oxygen mask ● 2–4 L/min via nasal cannulae; however, a mask is preferable if hypoxic and/or mouth breathing ● Over 60% oxygen with persistently low sats (<90%) use a non-rebreathe mask to administer constant flow of high concentration oxygen ● CPAP is useful with profound hypoxaemia once pneumothorax excluded Humidification ● Consider cold or heated humidification ● Heated is better for tenacious secretions or severe bronchospasm Treat the cause, e.g. ● If primary respiratory problem, treat this bronchospasm, sputum ● If primary problem is cardiac or renal, discuss with the retention, volume loss medical team

114 Management of respiratory failure Table 9.2 Continued Advice Common treatments Increased work of breathing ● Use airway clearance techniques if needed ● Positioning is essential to reduce breathlessness and improve ventilation perfusion matching ● IPPB may be useful (with a high flow rate) to rest the muscles and improve efficacy of other treatments Table 9.3 Common issues in hypoxia Common issues Advice Bronchopneumonia ● Ensure medication is optimized (oxygen, analgesia, bronchodilators, antibiotics, etc.) ● Positioning to decrease work of breathing ● Airway clearance techniques ● Humidification Acute lobar pneumonia ● During the unproductive phase advice on positioning may reduce WOB 9 ● CPAP is useful for hypoxaemia ● Sputum clearance is only indicated if the patient becomes productive ● Pneumocystis jiroveci (previously P. carinii) pneumonia (PCP – common in immunosuppressed patients, e.g. HIV) presents with profound hypoxia. CPAP is effective; however, pneumothorax is common – CXR is essential Pulmonary embolus ● Physiotherapy is not indicated. CPAP may help with severe hypoxaemia Pulmonary fibrosis ● Present with profound hypoxaemia. Humidified CPAP is effective ● Ensure sufficient oxygen is available when CPAP removed Pulmonary oedema ● CPAP is effective in treatment of pulmonary oedema. If hypotensive, check that BP does not drop with increased intrathoracic pressure. NIV (pressure support with EPAP) may be useful in the patient tiring on CPAP CO2 retention ● Acute CO2 retention is not a reason to reduce the FiO2 unless patients have evidence of acute-on-chronic CO2 retention secondary to chronic respiratory disease ● This can be diagnosed by interpretation of recent blood gas results, assessing pH, in relation to PaCO2, standard bicarbonate and base excess. Only this group of patients require judicious oxygen administration (24–28%), which should be prescribed accordingly

Management of respiratory failure 115 Table 9.3 Continued Common issues Advice Fatigue ● Hypoxaemic patients may start to fatigue. This is seen by a rising PaCO2 – type II failure. An important clinical sign requiring immediate attention. See below Chronic chest patients ● Patients with longstanding chest disease may have a regular chest clearance routine, e.g. cystic fibrosis, bronchiectatic patients ● Discuss and mould your treatment plan to fit their existing regimen with current physiotherapy problems Renal failure ● Patients in renal failure may present with ↑WOB ● ABGs will show metabolic acidosis, generally with some respiratory compensation – i.e. ↓CO2 (due to high RR) ● Pulmonary oedema and pleural effusion may be present Distended abdomen, e.g. ● Positioning in alternate side-lying or well-supported high pancreatitis, ascites side-lying is useful ● Standing if possible 9 Oesophageal varices ● Dilated blood vessels in oesophagus may rupture with increased pressure ● Care with coughing; suction contraindicated ● Prevent chest infection by positioning, teach huff, mobilize if able HYPERCAPNIA (TYPE II RESPIRATORY FAILURE/VENTILATORY FAILURE) Acute ventilatory failure can be caused by problems in several systems other than the respiratory system. Retention of carbon dioxide reflects hypoventilation. This is caused by a reduction in the extent and efficiency of gas mixing in alveoli and is primarily caused by inadequate alveolar ventilation. Any pathology affecting tidal volume and respiratory rate will affect gas mixing in the alveoli. A slight rise in arterial CO2 will produce a response – increasing ventilation by a rise in either respiratory rate, tidal volume or both. If this response is marked and the respiratory rate is >25/minute the work of breathing is high. The increased muscle work cannot be sustained for long periods and respiratory muscles begin to fatigue. In this case, patients develop a rapid shallow breathing pattern whereby tidal volume is reduced resulting in an inability to move little more than dead space volume (e.g. 150–200 ml). This means that CO2 cannot be adequately

116 Management of respiratory failure ‘washed out’ of the lung resulting in CO2 retention. This causes the following signs and symptoms: ● A surfeit of hydrogen ions producing a respiratory acidosis. ● Agitation and acute confusion. ● Patients may look flushed and peripherally dilated with a ‘bounding’ pulse (CO2 is a potent vasodilator). ● Patients may exhibit hand tremor known as CO2 related ‘flap’. ● When CO2 retention is profound, the patient is drowsy and difficult to rouse and respiratory rate is often reduced (<10 breaths per minute). This is CO2 narcosis which is a likely cause of CNS depression. NB: If the GCS is equal to or less than 9, the patients may not be able to protect their airway, so anaesthetic advice should be sought. Intubation and invasive mechanical ventilation may be indicated, especially with primary neurological pathology. See Table 9.4 for causes of acute ventilatory failure. Table 9.4 Causes of acute ventilatory failure 9 Causes of acute hypoventilation Explanation and carbon dioxide retention (acute ventilatory failure) ● Opiates used for pain relief, sedation and drug abuse. Check renal function if on small dose and CNS depression patient appears drowsy. Tell-tale sign is the presence of pinpoint pupils bilaterally ● Alcohol ● Head injury Respiratory disease ● Fatiguing respiratory muscles due to ↑work of Neuromuscular blockade breathing with a rapid shallow pattern ● Poor functioning respiratory membrane ● Oxygen >28% in chronic CO2 retaining patients ● Anaesthesia ● Ingestion of poison Muscle weakness – inability to ● Muscle diseases sustain increased respiratory ● Fatigue loads ● Long-term steroids ● Metabolic abnormalities (renal, liver impairment) Loss of integrity/restriction of ● Pain the chest wall – poor ● Circumferential burns to the thorax pulmonary mechanics ● Thoracic trauma ● Thoracic cage deformity (kyphoscoliosis) ● Previous thoracic surgery

Management of respiratory failure 117 Table 9.4 Continued Causes of acute hypoventilation Explanation and carbon dioxide retention (acute ventilatory failure) ● Upper motor neurone lesions (CVA, head injury) may affect respiratory rhythm and pattern Neurological impairment ● Lower motor neurone lesions (polio, multiple sclerosis, motor neurone disease, etc.) ● Neuromuscular junction (myasthenia gravis) ● Problems as for muscle weakness (above) TREATMENT OF HYPERCAPNIA 9 Treatment of ventilatory failure usually requires respiratory support in order to increase tidal volume and/or respiratory rate (i.e. minute ventilation) (Table 9.5). This can be intubation and ventilation or non-invasive ventilation (NIV) with a face mask. NIV is the treatment of choice for patients with acute ventilatory failure with a GCS > 9–10, provided there is no primary neurological pathology and they can protect their airway. For patients with chronic respiratory disease if the poor Table 9.5 Common treatments for hypercapnia Common treatments Advice Identify and ensure ● If the patient is on an opiate infusion, assess sedation treatment of the cause status especially in the elderly or patients with reduced of the hypoventilation renal/liver function as they will not be able to excrete opiates at a normal rate. In discussion with the medical team opiate infusions should be reduced or stopped, and reversing agents (e.g. naloxone) administered in severe cases. Alternative pain control should be found ● Severe bronchospasm and sputum retention need immediate, careful treatment ● If the cause is untreatable, e.g. Guillain-Barré, ventilation must be considered The primary treatment ● If respiratory rate is high this can only be achieved by for acute, severe CO2 increasing tidal volume. In order to do this assisted retention is to increase ventilation of some form is needed, e.g. IPPB, NIV the minute ventilation, ● IPPB will ↓WOB and ↑TV, thereby ↑O2 and ↓CO2, increasing without an increase in efficacy of cough (due to greater TV) during treatment. NIV the total work of will offer the same effect continuously breathing ● If sputum retention is the cause, short regular treatment is invaluable, incorporating IPPB, manual techniques, assisted cough and positioning

118 Management of respiratory failure Table 9.5 Continued Common treatments Advice Non-invasive ventilation ● Patients who do not respond to the above strategies may retain CO2 and become acidotic. Non-invasive ventilation 9 (NIV) should be considered if the resources and training are available; otherwise full ventilation will need to be discussed ● NIV allows correction of CO2, acid–base balance by increasing alveolar ventilation. NIV offloads some of the work of the respiratory muscles, allowing a degree of respiratory muscle rest. NIV is a mode of respiratory support rather than a treatment modality and is tolerated for protracted periods a. the system should be set up according to local hospital policy and you should be specifically trained and competent to do so b. check for contraindications c. discuss settings with the medical team d. correct mask fitting is essential for effective NIV: – leave false teeth in situ to maintain normal facial shape and tone – watch for potental leaks, e.g. around NG tubes – prevent tissue breakdown on the bridge of the nose, by ensuring good fit – avoid air blowing into the eyes e. Consider the need for additional humidification to prevent bronchospasm, secretion retention and further exacerbation of hypercapnia f. Entrain supplemental oxygen through the inspiratory limb of the ventilator in preference to a side port on the mask, and measure with an oxygen analyser g. Set the required minimum respiratory rate in case of complete apnoea due to oxygen therapy h. Monitor regularly for mask leaks, discomfort, claustrophobia, skin damage and gastric distension i. Discuss a management plan with the nursing staff, including how often to come off for drinks, cough, pressure area care, etc. j. Ensure repeat gases are taken 20–30 minutes after stabilization to check effect upon the hypercapnia/ acidosis. If no effect check with medical team and change settings in line with agreed local policy k. Gradually reduce time spent on treatment as indicated by the clinical condition and as independent ventilation becomes more effective at maintaining gas exchange ● Full ventilation has the same effect

Management of respiratory failure 119 GCS is as a result of CO2 narcosis (look for evidence of elevated CO2 and bicarbon- ate ions in the blood gas) – then a trial of NIV may be appropriate, provided a plan has been put in place for intubation if there is no improvement in the first 30 minutes and it is carried out in the intensive care unit with early access to intubation. In mild hypercapnia, intermittent positive pressure breathing (IPPB) may be adequate to improve alveolar ventilation in the short term – as this is an intermittent treatment it is unlikely that severe hypercapnia will be reversed. See Table 9.6 for common issues in hypercapnia. Remember acute ventilatory failure can be caused by problems in several systems other than the respiratory system. However, it is important to stress that it may be caused by an acute deterioration of a chronic condition – it is helpful to read the patient’s old notes to establish what the patient’s usual status is – see section on chronic ventilatory failure. 9 Table 9.6 Common issues in hypercapnia Common issues Advice Low pH ● Once pH dips below normal range urgent treatment from the whole team is needed Call to A&E ● You may be called to resus in A&E as this client group benefit from timely physiotherapy intervention ● Do not be scared by this – treat it as a ward, with more help on hand ● Start your treatment here No access to IPPB, CPAP, ● If a patient requires positive pressure for treatment NIV in ward area and no other treatment options remain, they must be moved to an appropriate area – the medical team should be able to arrange this ● If your hospital does not have access to CPAP, IPPB or NIV treat the patient to the best of your ability using the techniques available to you. Often excellent results are possible. If the patient needs more assistance ICU support will be required – inform the medical staff as to the limitations of your treatment High probability of death ● If the team establish that death is the most likely outcome, the need for treatment must be weighed up against the discomfort felt by the patient and their needs, e.g. time with family

120 Management of respiratory failure CAUSES OF CHRONIC CO2 RETENTION (CHRONIC VENTILATORY FAILURE) Patients with chronic respiratory disease may have chronic CO2 retention. This is identified from blood gas analysis where the PaCO2 is >6.5 kPa, the pH is normal and the bicarbonate (HCO3) is also elevated above 28 mmol/l. If these patients develop ‘acute-on-chronic respiratory/ventilatory failure’, they will retain more CO2 but the pH will fall as there will be insufficient time for the kidneys to retain bicarbonate ions to correct the acidosis. NIV is the treatment of choice in this situation, bearing in mind the cautions mentioned above. See Table 9.7 for causes of chronic ventilatory failure and Table 9.8 for common medications. Table 9.7 Causes of chronic ventilatory failure Respiratory disease ● Inadequate alveolar ventilation due to fatiguing respiratory muscles; inadequate surface area for gas exchange Cardiac disease ● Cardiac failure (LVF/CCF) and pulmonary oedema increase respiratory work, with poor oxygenation 9 of the respiratory muscles Neurological diseases ● Inadequate respiratory muscle strength and endurance Muscle problems ● As for neurological, above ● Profound malnutrition ● Hyperinflation alongside respiratory disease Sleep-related breathing disorders ● Severe, longstanding obstructive sleep apnoea, nocturnal hypoventilation/central sleep apnoea Table 9.8 Common medications Common medication effects Examples of medication Bronchodilators ● Nebulized: salbutamol, terbutaline, ipratropium bromide ● Intravenous: salbutamol, aminophylline Corticosteroids ● Nebulized: beclometasone ● Oral: prednisolone Diuretics ● Furosemide (frusemide) Anticoagulants ● Tinzaparin, heparin Anti-arrhythmics ● Digoxin, amiodarone, adenosine

Management of respiratory failure 121 9 Key messages ● Treatment must be aimed at the cause of the hypoxia and/or hypercapnia so that deranged gas exchange can be corrected and work of breathing reduced. ● Respiratory support in the form of oxygen and positive-pressure techniques can support the patient while physiotherapy techniques may expedite recovery. Further reading BTS Guideline (2002) Non-invasive ventilation in acute respiratory failure. Thorax 57: 192–221. Davidson C, Treacher D (eds) (2002) Respiratory critical care, 1st edn. London: Edward Arnold. West JB (2004) Respiratory physiology: the essentials, 6th edn. London: Lippincott Williams & Wilkins. West JB (2007) Pulmonary pathophysiology: the essentials, 7th edn. London: Lippincott Williams & Wilkins.



CHAPTER 10 Calls to adult intensive care Rachel Devlin The purpose of this chapter is to highlight different terminology, equipment and specific issues pertinent to the intensive care patient. This chapter will cover: ● Considerations in the assessment of the ICU patient ● The environment ● Common pathologies ● Physiotherapy management. Calls to an intensive care unit (ICU) can be nerve-wracking due to the complexity of the environment, the variety of pathologies encountered and the severity of the patient’s condition. However, remember that this is a safe environment for you as all ICU patients are closely monitored. There is a higher proportion of nursing staff to patients, and staff are highly skilled and can offer a wealth of advice and assistance in an on call situation, e.g. explaining unfamiliar terminology. It is important to remember that critically ill patients may be anywhere in the hospital. As such, critical care should be viewed as a concept, rather than a loca- tion. You may be the first person to locate such a patient and in that case you should not be afraid to call for help. Many units have recognized this and have developed ‘critical care outreach teams’ to support staff. You should check your local policies to see if your unit has an outreach team and how to access them. SPECIAL CONSIDERATIONS FOR ASSESSING ICU PATIENTS Remember! The basic components of respiratory assessment remain the same regardless of whether the patient is on ICU or on a ward. See Chapter 2. Using a logical format allows you to identify whether the patient has (or is at risk of devel- oping) loss of lung volume, sputum retention or increased work of breathing leading to respiratory failure (see also Chapters 6–9).

10 124 Calls to adult intensive care GENERAL ● What is the patient’s global stability and response to handling? ● What has happened since admission/last treatment (e.g. intubation, lines inserted) ● What physiological parameters are the medical team working towards? ● Note the equipment attached to the patient, e.g. drips and drains. ● Are there any limitations to movement or positioning (e.g. due to attachments, equipment or spinal stability – see Chapter 14). CVS ● What is the patient’s heart rate/rhythm? Is it compromising their blood pressure? What effect is your treatment likely to have on this? ● Is BP stable? Are they on any inotropic support? CNS ● Is the patient sedated? Are they on any paralysing agents? ● What is the patient’s level of consciousness? (sedation scoring, AVPU, GCS) ● Is analgesia sufficient for full assessment and treatment? ● Is there any neurological deficit evident? If so, is swallow/cough reflex affected? (see Chapter 14). BIOCHEMISTRY ● What is Hb? ● Is clotting deranged? (look at platelets/INR/PT/APTT) ● Are there signs of infection/sepsis? (WCC/CRP/lactate) RENAL ● What is current urine output? Overall fluid balance? ● Is the patient on any renal support? (diuretics, haemofiltration) RS ● Mode of ventilation and method of delivery? ● Ventilator settings? ● Level of oxygen? Saturations? ● Does the patient have a cough? Sputum on suction? Colour, volume and consistency? Clearing easily with suction? ● Are there chest drains in situ? What are they there for?

Calls to adult intensive care 125 10 A few additional factors need to be considered before you continue: ● Anxiety ● Explain all interventions to the patient regardless of their sedation level in order to minimize anxiety – there is good evidence that patients can hear what is happening. ● Relatives ● Friends and relatives will find this environment very stressful. This can manifest itself in many ways. Always remain calm and professional, listen to what they have to say – they can be an advocate for you with the patient. But remember you are there to treat the patient and do what you and the team feel is most appropriate for their care. ● Make sure you know who you are talking to and respect your patient’s confidentiality. ● Discuss your role with the patient’s relatives, but try to avoid having conversations about medical plans, prognosis, etc. This is the role of ICU staff. ● Expectations ● Patients in ICU are by definition critically ill; therefore there may be a high probability of death. Try to be realistic in your expectations of yourself. ● Balance the probable benefit of your treatment against the discomfort, time and energy that it may require of the patient. ● On occasion, when a patient has been weaned from support and extubated, the decision is made that the treatment will not be escalated should their condition deteriorate. In a small number of cases where the patient will not survive their illness, the ET tube may be removed and the patient made comfortable as part of the palliative process. ● The unfamiliar ● When encountering unfamiliar pathologies with an uncertain prognosis, it is important not to pre-judge the outcome of their ICU stay. Ask the nursing staff what to expect of the underlying pathology and consider any potential contraindications for physiotherapy treatment. During your induction to on call you should familiarize yourself with the equipment commonly used within ICU. Before approaching the patient, note the equipment, lines, etc. that are attached to the patient and the precautions/care you should take. Remember! If you are unsure of any equipment or lines ask for help/explanation from ICU staff.

126 Calls to adult intensive care THE ENVIRONMENT ICU has many pieces of equipment – Table 10.1 gives a brief summary of some of the common items you will see. With lots of equipment come lots of different alarm systems. For equipment such as infusion pumps it is vital you do not switch them off. However, it is helpful to nursing staff if you can identify the cause of the alarm. For monitoring and ventilators Table 10.2 highlights some of the common causes of alarms in ICU and how you should manage them. Do not switch off alarms unless you are com- petent to identify the cause and manage appropriately. If in doubt, ask! Table 10.1 ICU equipment Explanation Equipment ● Inserted via radial, brachial or dorsalis pedis Arterial line – blood pressure arteries monitoring ● Care with positioning to avoid disconnection or kinking of lines (may make the trace unreliable) ● Liaise with nursing staff regarding reliability of the trace ● Blood pressure cuffs may also be used 10 ECG electrodes – heart rate and ● Take care with techniques that may disrupt the rhythm monitoring trace and set off the alarms, e.g. manual techniques ● Always remember to check the ‘stickies’ if the trace changes CVP (central venous pressure) ● Commonly inserted in the internal jugular or line – monitors pressure in the subclavian vein right side of the heart ● Drugs may be administered via the CVP line; if so the measurement will be inaccurate. Take care not to kink the line during turning as drug delivery may be affected ● Risk of pneumothorax during insertion; therefore ensure that patient has a CXR prior to using positive pressure adjuncts, e.g. IPPB, MHI Invasive cardiac monitoring/ ● Refer to Chapter 15 equipment (e.g. PA catheter, ● Check with staff on stability of patient and PiCCO/LiDCO, intra-aortic balloon pump (IABP), pacing wires) limitations to movement/positioning ● There are similar risks with the insertion of PA catheters as with CVP lines Invasive neurological monitoring/ ● Refer to Chapter 14 equipment (e.g. ICP bolt, ● Check with staff on stability and limitations to extraventricular drains (EVD) or cerebral function monitors (CFM)) positioning

Calls to adult intensive care 127 Table 10.1 Continued Equipment Explanation Haemofiltration (HF) – renal ● Vas-Cath (a large-bore double-lumen cannula) failure. May also be documented inserted into the subclavian or internal jugular as CVVHF or CVVHD vein (for neck), or femoral veins (for groin) ● Take care not to kink lines – will affect function of machine. Do not flex the hip greater than 30–45º if femoral line ● Check with staff on stability and other limitations to positioning ● There will be changes in overall fluid status with patients on renal support that may predispose them to cardiovascular instability Airways ● Endotracheal tube used initially Endotracheal tube (may be oral ● Nasal ETT may suggest a difficult intubation – so or nasal), trachesotomy tube take care ● Tracheostomy may be used to wean from 10 mechanical ventilation. See tracheostomy section in Chapter 13 ● Ventilated patients will have a cuffed airway in place. If a patient is able to vocalize or there are audible oral noises, inform the nursing staff as there may be a cuff leak which may affect ventilation Ventilators ● Different manufacturers of ventilator have different Be aware of the different types of names for the modes of ventilation (e.g. BiPAP, ventilator in use in your hospital. PRVC, ASB, etc.). Often the full name will give you It is of note that a variety of a clue as to the type of ventilation this is ventilatory parameters can be changed in order to optimize gas ● Controlled modes of ventilation – the patient exchange and minimize the makes little or no respiratory effort. This may potential damage to the lungs indicate a more acute or severe condition, e.g. head injury or sepsis ● Supported modes of ventilation allow the patient to trigger the ventilator, namely that they are able to initiate some breaths. This indicates that the patient’s condition is improving or less severe. These modes can be used while weaning ventilation (decreasing respiratory support) ● Modern machines will allow a patient to breathe on top of a controlled mode of ventilation. To see if a patient is doing this, look at the set breathing rate and then the actual breathing rate on the ventilator Non-invasive ventilation/CPAP ● See Chapter 9

10 Table 10.2 Common causes of alarms in an ICU and their management 128 Calls to adult intensive care Problem Potential causes Physiotherapy management Reduced lung volumes ● Leak in circuit ● Check connections in circuit May alarm as: ● Dislodged ETT ● Consider repositioning ● Decreased tidal volume ● Excess water in circuit ● Suction or further physiotherapy intervention ● Decreased minute volume ● Sputum plug ● Patient may require increased FiO2 ● Decreased SpO2 ● Acute lung injury ● Increased peak airway pressure Increased work of breathing ● Bronchospasm ● Analgesia, reassurance, sedation or increased May alarm as: ● Patient waking/biting on tube ventilatory support ● Decreased tidal volume ● Patient waking up and making increased ● Decreased minute volume ● Nebulized bronchodilators ● Increased respiratory rate respiratory effort ● Increased respiratory rate, e.g. due to pain, anxiety or fatigue Sputum retention ● Sputum plug ● Suction or further physiotherapy intervention May alarm as: ● Patient waking up/coughing ● Patient may require increased FiO2 ● Increased peak airway pressure ● Decreased SpO2 ● Decreased tidal volume Respiratory failure ● Could be any combination of the above ● Needs review of ventilator settings

Monitor alarming ● Unreliable arterial line trace ● If unreliable, use blood pressure cuff Decreased blood pressure ● Kinked lines ● Ensure lines are patent for effective delivery of drugs, ● Due to bleeding Increased blood pressure ● Following nursing intervention, e.g. turning e.g. inotropes Increased heart rate ● Patient may require intravenous fluids/surgical opinion ● During physiotherapy intervention, e.g. MHI ● Observe if BP returns to normal. If not, return patient or manual techniques to supine. If low BP persists, patient may require ● Due to increase/bolus of sedation intravenous fluids or inotropes ● Stop technique and allow patient to settle; BP should recover quickly. If not, discuss further intervention with nursing staff. One treatment at a time may be possible or there may be a medical solution to support BP during treatment ● Administer intravenous fluids or decrease sedation if appropriate ● Pain ● Analgesia Calls to adult intensive care 129 ● Anxiety ● Sedation or reassurance ● Infection ● Investigation and treatment of underlying cause ● Decreased blood volume, e.g. bleeding, ● Patient requires medical review haemofiltration ● Analgesia ● Pain ● Sedation or reassurance ● Anxiety 10

10 Table 10.2 Continued Potential causes Physiotherapy management 130 Calls to adult intensive care Problem ● Patient may require medical review Decreased heart rate ● Due to medication, e.g. beta-blockers, sedatives ● Monitor response to further interventions and discuss with medical team ● Due to vagal stimulation, e.g. following suction or movement of ETT ● Patient may require anti-arrhythmic drugs, e.g. amiodarone, or cardioversion to restore sinus rhythm Arrhythmias, e.g. atrial fibrillation ● Hypoxia (ensure nursing staff are aware of ● Sepsis ● Treatment of underlying cause any change in ECG trace) ● Check reliability of trace (i.e. HR from pulse oximeter Decreased SpO2 ● Unreliable trace and ECG trace should match). If poor, relocate probe, e.g. to toes, earlobes ● Sputum retention ● Decreased lung volume or V/Q mismatch ● Suction or further physiotherapy intervention ● Consider repositioning or further physiotherapy ● Fluid overload intervention ● Diuretics, inotropes, renal support ● Patient may require increased FiO2

Calls to adult intensive care 131 COMMON PATHOLOGIES/CONDITIONS IN ICU Table 10.3 summarizes some of the common pathologies and conditions seen within the ICU. As part of your assessment you will also note that the patient may be receiving a number of drugs with which you are unfamiliar. Common drugs encountered in intensive care are described in Appendix 4. Bringing together all the information that you have gathered from your assessment will help you to identify the patient’s individual problem and allow you to develop a treatment plan (Table 10.4). Table 10.3 Common ICU pathologies and conditions ARDS (acute ● Syndrome characterized by reduction in lung compliance and respiratory distress need for high PEEP and oxygen requirements but as it is an syndrome)/ALI (acute interstitial pathology secretions are not generally a problem lung injury) ● Caution with hands-on techniques as you do not want to de-recruit lung units (i.e. lose the splinting effect of the 10 ventilator PEEP) ● Treatment may consist of positioning only, e.g. prone-lying to optimize gaseous exchange ● If secretions become a problem ensure adequate humidification along with other techniques to improve sputum clearance Sepsis – systemic ● Normal WBC = 4–11 × 109/L; ↑WBC indicates infection inflammatory response ● CVS instability, e.g. decreased BP, will occur and patient syndrome (SIRS) may require cardiac support drugs or fluid management to maintain adequate perfusion ● Positioning or MHI may be contraindicated as these may compromise BP ● Urine output may decrease leading to fluid overload and pulmonary oedema. This will compromise oxygenation and the patient may require high FiO2 and increased PEEP ● If there are signs of pulmonary infection, try one treatment at a time, e.g. side-lying, and monitor the patient’s CVS response Unilateral lung ● Self-ventilating patient – See Chapter 12 pathology, e.g. ● Intubated patients – Remember V/Q. IPPV changes the pneumonia dynamics of ventilation and air is forced into area of least resistance. Therefore the airways which are open more tend to get overstretched. In a side-lying patient the non- dependent area (upper lung) receives greater ventilation. Perfusion is unchanged in the ventilated patient

132 Calls to adult intensive care 10 Table 10.3 Continued ● If the affected lung is dependent, desaturation may occur due to poor perfusion. If it is non-dependent, desaturation Head injuries, may occur because the disease process limits gas exchange neurosurgery and secondary to secretions. You need to assess each patient spinal cord injuries on an individual basis and establish appropriate positions for Spinal fractures/ treatment, which may be different to the position you leave orthopaedic trauma the patient in Rib fractures/flail ● Refer to local hospital guidance on management segment/sternal ● See Chapter 14 fractures/lung contusions ● See Chapters 13 and 14 Burns ● Long bone fractures may cause fat emboli leading to type I respiratory failure ● Log rolling only until a full set of spinal films has been performed and the spine cleared; medical staff must document if patient can be positioned in any position other than supine ● Note orthopaedic instruction for peripheral fractures ● Be aware of fracture sites ● For management see Chapter 15 ● Ensure that the patient has effective pain relief and adequate humidification as secretions may be thick and difficult to clear ● Early, regular chest clearance is vital to remove soot (etc.) particles from the lungs. Soot around the nose and mouth is suggestive of inhalation injury which results in oedema and sputum ● Patients with large-scale burns will require rapid fluid replacement and so are prone to pulmonary oedema ● If stridor occurs, seek urgent medical advice due to risk of airway obstruction ● Postural drainage is contraindicated in the presence of head/neck oedema ● Check local policies with regard to movement and manual techniques over skin grafts. Some units allow this once the graft is established provided that the graft is healthy and there is thick padding over the affected area. Check with the on call team covering the specialty which undertook the surgery

Calls to adult intensive care 133 Table 10.3 Continued ● Escharotomy of the chest wall; effective chest care is essential – however, analgesia is vital ● Burns patients are immunosuppressed, so it is vital to adhere to infection control policies ● Many units require that passive movements to affected areas are continued for burns patients at weekends – check local policy Clotting disorders ● If INR >1.0 (associated with anticoagulants or liver dysfunction) or in the presence of DIC (disseminated intravascular coagulation), bleeding may occur leading to 10 cardiovascular instability ● Secretions may be blood stained and care should be taken if performing suction to minimize trauma. Manual techniques may be contraindicated ● If INR <1.0 there will be a predisposition to clotting, e.g. DVT, PE ● A falling platelet count may be a sign of sepsis. Low platelets predispose to bleeding and therefore care should be taken during all interventions to minimize trauma to the patient, e.g. when repositioning the patient Postoperative patients ● Effective pain relief is essential to ensure patient compliance with treatment ● Important to observe surgical instructions regarding positive pressure adjuncts, positioning and mobilization ● See Chapter 13 Respiratory medical ● See Chapter 12 patients ● Aim to prevent patient fatigue by management of increased work of breathing and sputum retention ● NIV may be considered. Setting up NIV may not be the role of the on call physiotherapist, so it is important to be aware of hospital policy Renal failure patients ● See Chapter 12 ● A patient may present with respiratory problems, e.g. increased RR, but blood gas analysis shows that it is a compensatory mechanism for a primary metabolic problem, e.g. acute renal failure ● Patient may be admitted for haemofiltration; see Chapter 12 ● Main problem is commonly pulmonary oedema leading to type I respiratory failure. This may respond to diuretics and CPAP

10 Table 10.4 Management of ICU problems 134 Calls to adult intensive care Problem Cause Physiotherapy management Further management Sputum clearance techniques Sputum Poor cough, pain, Decrease sedation, ensure adequate analgesia, retention dehydration, fatigue increase respiratory support, e.g ↑pressure support Bronchospasm Previous respiratory disease, Sputum clearance techniques. Bronchodilators, diuretics, haemofiltration sputum retention, fluid Positions to relieve breathlessness, overload, renal failure, anxiety reassurance Lobar collapse Sputum plug, migration of ET Sputum clearance techniques. Reintubation, bronchoscopy. Rehydration tube, position in bed Mobilization, e.g. sitting out Pulmonary Cardiac or renal failure Physiotherapy is NOT indicated for Inotropic support, e.g. epinephrine; diuretics, e.g. oedema pulmonary oedema furosemide. Fluid restriction. Haemofiltration Pulmonary Physiotherapy is NOT indicated for a Anticoagulation, TED stockings embolus (PE) PE. Do NOT mobilize patient without discussing with doctors Pleural effusion Cardiac/renal failure. Fluid Physiotherapy is NOT indicated for a Diuretics, intercostal chest drain. overload. Malignancy pleural effusion, although patient See Chapter 18 may respond to positions to relieve breathlessness if symptomatic Pneumothorax Spontaneous, e.g. Marfan Encourage mobilization Analgesia. Intercostal chest drain if symptomatic. syndrome See Chapter 18 Traumatic, e.g. stabbing Fatigue As described previously Sputum clearance techniques, positions Treatment of underlying cause. to decrease breathlessness, Non-invasive ventilation, intubation and ventilation, reassurance increasing respiratory support. Sedation, e.g. propofol

Calls to adult intensive care 135 10 Key messages ● Approach assessment of the ICU patient in the same systematic and logical format that you would use to assess a ward patient. ● Work closely with the nursing and medical staff. ● Communicate the outcome of your assessment and treatment succinctly. ● Don’t be afraid to ask questions. ● Don’t be scared! Acknowledgements The author would like to acknowledge the input of Sara Smailes in the burns section of this chapter. Further reading Bersten A, Soni N, Oh TE (eds) (2003) Oh’s intensive care manual, 5th edn. Oxford: Butterworth Heinemann. Hough A (2001) Physiotherapy in respiratory care: a problem solving approach to respiratory and cardiac management, 3rd edn. Cheltenham: Stanley Thornes. Pryor JA, Prasad SA (eds) (2002) Physiotherapy for respiratory and cardiac problems, 3rd edn. London: Churchill Livingstone. Singer M, Webb A (eds) (2005) Oxford handbook of critical care, 2nd revised edn. Oxford: Oxford University Press.



CHAPTER 11 Calls to paediatric ICU (PICU) Elaine Dhouieb Paediatric intensive care covers a wide range of conditions and ages from prema- ture neonates to 16-year-olds. Physiotherapists should be aware of continuing lung development into teenage years. Chest clearance should be used only where indi- cated. Careful assessment and discussion with medical and nursing staff is needed. Clinical signs may be much more discreet, especially in infants. Intensive care units are high-technology, frightening places for most people. Take advantage of skilled medical and nursing staff for help and advice. It may be more difficult to gain the cooperation of a small child in treatment, and consent issues must also be considered. Parents will have 24-hour access and in most units will not be asked to leave during treatment. Their needs, fears and anxieties must also be considered. Tables 11.1–11.4 detail the aims of physiotherapy in the PICU, inappropriate calls to the PICU, common PICU issues and PICU treatment precautions, respectively. CONDITIONS Patients are admitted to PICU with a wide range of conditions. They may have a wide range of congenital or other underlying conditions to be considered (Table 11.5). A proportion of children have severe neurological conditions which predis- pose them to respiratory complications. THE CALL OUT ● Information gathered will be similar to that in adult ICU. ● Work closely with the nursing staff; they are exceptionally skilled at handling sick children. ● Ask lots of questions (see Chapter 4). ● Never be afraid to ask for help.

138 Calls to paediatric ICU (PICU) Table 11.1 Aims of physiotherapy on PICU Aims of treatment ● Remove secretions ● Re-inflate areas of atelectasis ● Reduce airflow obstruction ● Improve gas exchange ● Decrease work of breathing ● Prevention of respiratory compromise Table 11.2 Inappropriate calls to PICU Potentially inappropriate calls Inhaled foreign body ● Physiotherapy may move the object further down the bronchial tree; do not treat until the child has had bronchoscopy to remove ● Reassess and treat as appropriate Epiglottitis, croup, stridor ● Unless the child is intubated physiotherapy techniques may increase swelling and compromise respiration 11 ● After extubation do not treat for at least 2 hours or if there is significant stridor Bronchiolitis ● In a self-ventilating infant with no other underlying condition physiotherapy does not add any benefit to good nursing care of positioning, hydration and suction ● The ventilated infant should be assessed and treated if indicated Whooping cough/pertussis ● In the acute phase of paroxysmal coughing, physiotherapy can initiate coughing which may compromise the child ● Only treat if there are retained secretions and the child is paralysed and sedated ● May have retained secretions after acute phase Extreme prematurity or low ● See Chapter 18 birthweight